Objective: A reduction of the Ca(2+)-independent transient outward potassium current (I(to)) in epicardial but not in endocardial myocytes of the left ventricle has been observed in cardiac hypertrophy and is thought to contribute to the electrical vulnerability associated with this pathology.
Methods: In the present study we investigated the molecular mechanisms underlying regional alterations in I(to) in hypertrophied hearts of spontaneously hypertensive rats (SHR) using the whole-cell patch-clamp technique, quantitative RT-PCR and heterologous expression of underlying ion channel subunits.
Results: I(to) was significantly smaller in epicardial myocytes of SHR than in Wistar-Kyoto (WKY) controls (11.
Recent studies showed that the Ca(2+)-independent transient outward current (I (to)) is very small or even not detectable in the porcine left ventricle. We investigated whether an altered molecular expression or function of voltage-dependent potassium channels belonging to the Kv4 sub-family and their ancillary Ca(2+)-binding beta sub-unit KChIP2, which contribute to the major fraction of I (to )in other species, may underlie this lack of a significant I (to) in the porcine left ventricle. RT-PCR analysis with degenerate primers showed that both Kv4 mRNA and KChIP2 mRNA are expressed in porcine left ventricular tissue and in isolated ventricular myocytes.
View Article and Find Full Text PDFRegulation of the epithelial sodium channel (ENaC) is important for the long-term control of arterial blood pressure as evidenced by gain of function mutations of ENaC causing Liddle's syndrome, a rare form of hereditary arterial hypertension. In Xenopus laevis oocytes expressing ENaC a spontaneous decline of ENaC currents over time, so-called rundown, is commonly observed. Mechanisms involved in rundown may be physiologically relevant and may be related to feedback regulation of ENaC by intra- or extracellular Na+.
View Article and Find Full Text PDFBackground: Tension of the abdominal wall in the inguinal region induced by Shouldice repair of an inguinal hernia is said to be responsible for elevated postoperative pain levels.
Patients And Methods: In 20 patients we recorded the inguinal tensile strength during closure of the hernial gap using a wound retractor equipped with strain gauges. Postoperative pain levels were scaled using a visual analogous score, and correlated with the tensile strength of the inguinal abdominal wall together with peak flow and forced expiratory volume in 1 s (FEV1) 8, 24, and 48 h after the time of operation.
Objective: To find out the effect of standardised stress on the load of the inguinal region.
Design: Experimental study.
Setting: Surgical university clinic, Germany.